Isolation of the Lateral Border Recycling Compartment Using a Diaminobenzidine‐Induced Density Shift

Sullivan, David P.; Rüffer, Claas; Müller, William A.

doi:10.1111/tra.12184

Cited by 13 publications

(19 citation statements)

References 36 publications

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“…Removal of this domain from VE‐cadherin or competition with a soluble RVDAE peptide allowed its entry into the LBRC. This explains why no unique proteins were found in the isolated LBRC and enriched proteins were associated with the cytoplasmic side . This study also demonstrated that the constituents of the LBRC move in concert during TEM; there is no separation of membrane enriched in PECAM or CD99 .…”

Section: Initiating Transmigration: Major Membrane Movementsmentioning

confidence: 75%

“…These studies confirmed that caveolin‐1 is not a component of the LBRC and revealed that in addition to VE‐cadherin, its associated catenins were also excluded from the LBRC. We were unable to identify any unique proteins in the LBRC; however, both IQ motif GTPase‐activating protein 1(IQGAP1) and vimentin were specifically enriched in the LBRC fraction .…”

Section: Initiating Transmigration: Major Membrane Movementsmentioning

confidence: 82%

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Transendothelial migration: unifying principles from the endothelial perspective

Müller

2016

Immunological Reviews

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144

131

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Summary Transendothelial migration (TEM) of PMN involves a carefully orchestrated dialogue of adhesion and signaling events between leukocyte and endothelial cell. This chapter will focus on the endothelial cells’ contribution to transmigration. The initiation of TEM itself generally requires interaction of PECAM on the leukocyte with PECAM at the endothelial cell border. This is responsible for the transient elevation of cytosolic free calcium ions in endothelium that is required for TEM and for recruitment of membrane from the lateral border recycling compartment (LBRC). TEM requires LBRC to move to the site at which TEM will take place and for VE-cadherin to move away. Targeting of the LBRC to this site likely precedes movement of VE-cadherin, and may play a role in clearing VE-cadherin from the site of TEM. The process of TEM can be dissected into steps mediated by distinct pairs of PMN/endothelial interacting molecules. CD99 regulates a step at or close to the end of TEM. CD99 signals through soluble adenylyl cyclase to activate PKA to trigger ongoing targeted recycling of the LBRC. Paracellular transmigration predominates (≥ 90% of events) in the cremaster muscle circulation, but transcellular migration may be more important at sites such as the blood brain barrier. Both processes involve many of the same molecules as well as recruitment of the LBRC.

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Section: Initiating Transmigration: Major Membrane Movementsmentioning

confidence: 75%

Section: Initiating Transmigration: Major Membrane Movementsmentioning

confidence: 82%

Transendothelial migration: unifying principles from the endothelial perspective

Müller

2016

Immunological Reviews

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144

131

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“…The LBRC is a reticulum of 50 nm vesicular structures that are connected to each other and to the plasma membrane at intervals along the cell borders [11]. The LBRC contains a representative selection of lateral border membrane with the exception of VE-cadherin [13,14], which is actively excluded [15]. Membrane from the LBRC is moved by kinesin molecular motors along microtubules [16] to surround the leukocyte during its passage across the endothelial border during paracellular migration [11] and through the cell during transcellular migration [13].…”

Section: Tem Itself Is a Multi-step Pathwaymentioning

confidence: 99%

Localized signals that regulate transendothelial migration

Müller

2016

Current Opinion in Immunology

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Transendothelial migration (TEM) of leukocytes is the step in leukocyte emigration in which the leukocyte actually leaves the blood vessel to carry out its role in the inflammatory response. It is therefore, arguably the most critical step in emigration. This review focuses on two of the many aspects of this process that have seen important recent developments. The adhesion molecules, PECAM (CD31) and CD99 that regulate two major steps in TEM, do so by regulating specific signals. PECAM initiates the signaling pathway responsible for the calcium flux that is required for TEM. Calcium enters through the cation channel TRPC6 and recruits the first wave of trafficking of membrane from the lateral border recycling compartment (LBRC). CD99 signals through soluble adenylate cyclase to activate protein kinase A to recruit a second wave of LBRC trafficking. Another process that is critical for TEM is transient removal of VE-cadherin from the site of TEM. However, the local signaling pathways that are responsible for this appear to be different from those that open the junctions to increase vascular permeability.

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“…The LBRC is a reticulum of interconnected membrane below the cell borders. It is defined by its function, as there are no identified unique markers (Sullivan et al, 2014). Membrane constitutively cycles between the border and this compartment evenly along the junctions between endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

“…Vascular endothelial cell specific cadherin (VE-cadherin), a major component of the endothelial cell border, is not present in the LBRC Sullivan et al, 2014). VEcadherin plays a central role in the formation and maintenance of adherens junctions and barrier function in endothelium (Dejana and Giampietro, 2012;Dejana et al, 2008;Vestweber et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Segregation of VE-cadherin from the LBRC depends on the ectodomain sequence required for homophilic adhesion

Feng

Sullivan

Han

et al. 2014

Journal of Cell Science

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The lateral border recycling compartment (LBRC) is a reticulum of perijunctional tubulovesicular membrane that is continuous with the plasmalemma of endothelial cells and is essential for efficient transendothelial migration (TEM) of leukocytes. The LBRC contains molecules involved in TEM, such as PECAM, PVR and CD99, but not VE-cadherin. Despite its importance, how membrane proteins are included in or excluded from the LBRC is not known. Immunoelectron microscopy and biochemical approaches demonstrate that inclusion into the LBRC is the default pathway for transmembrane molecules present at endothelial cell borders. A chimeric molecule composed of the extracellular domain of VEcadherin and cytoplasmic tail of PECAM (VE-CAD/PECAM) did not enter the LBRC, suggesting that VE-cadherin was excluded by a mechanism involving its extracellular domain. Deletion of the homophilic interaction domain EC1 or the homophilic interaction motif RVDAE allowed VE-CAD/PECAM and even native VEcadherin to enter the LBRC. Similarly, treatment with RVDAE peptide to block homophilic VE-cadherin interactions allowed endogenous VE-cadherin to enter the LBRC. This suggests that homophilic interactions of VE-cadherin stabilize it at cell borders and prevent entry into the LBRC.

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Isolation of the Lateral Border Recycling Compartment Using a Diaminobenzidine‐Induced Density Shift

Cited by 13 publications

References 36 publications

Transendothelial migration: unifying principles from the endothelial perspective

Transendothelial migration: unifying principles from the endothelial perspective

Localized signals that regulate transendothelial migration

Segregation of VE-cadherin from the LBRC depends on the ectodomain sequence required for homophilic adhesion

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